The mechanistic relationships between the early inflammatory response and subsequent fibrosis seen after radiation exposure were studied in rats given X-ray doses of either 2000 or 5000 rad to standardized fields of the inner thigh. The animals were further subdivided into those receiving no additional treatment and those depleted of complement with cobra-venom factor. The results are consistent with the hypothesis that two mechanisms are responsible for the increases in extravasation rate and vascular injury seen after irradiation. First, direct cytocidal damage; second, chemically mediated, possibly complement-dependent, mechanisms. In addition, these data suggest that both direct and indirect damage to the vasculature play a role in influencing the subsequent late-radiation-induced fibrosis.

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